A system of practical medicine. By American authors. Vol. 2

by Unknown

The occasional presence of sugar in the urine of gouty persons has already been noted. I have repeatedly observed this symptom in the urine of gouty dyspepsia. It occurs more commonly in obese subjects, and is usually intermittent and easily controlled by dietetic restrictions. In these cases it is not necessarily associated with a very large amount of urine. In chronic gout and in connection with the granular kidney a more serious form of glycosuria is occasionally observed. Under these circumstances it increases largely the polyuria which is characteristic of gouty nephritis, and is sometimes overlooked because it occurs in a urine of a low density, often not more than 1.010. It is not controlled by diet to the same extent that it is in the cases previously described, and is in my experience a prognostic sign of bad import.

Some of the most distressing symptoms to which gouty persons are especially liable are those connected with the passage of gravel from the kidney to the bladder. Where gravel alone passes, it may cause little uneasiness, and the fact is only recognized through the discovery of blood in the urine in connection with uric acid or calcium oxalate crystals. When, however, the sand forms concretions in the pelvis of the kidney, their dislodgment and passage through the ureter are accompanied by the well-known agonies of renal colic.

Dysuria is a symptom from which gouty persons often experience much inconvenience and suffering. It is usually associated with extremely acid urine of high density containing crystalline sediments. It may manifest itself only in frequent and painful micturition, or it may be associated with such a degree of vesical tenesmus as to cause retention and necessitate the use of the catheter.

DIAGNOSIS.—If the term gout be restricted to that form of arthritis in which an excess of urates is found in the blood with tophous deposits in the affected joints, the cartilages of the ear and nose, and in the subcutaneous connective tissue, then the diagnosis of this disease is a simple one. It is a disease with a pathognomonic sign. But if the pathology of gout consists rather in a more complex morbid condition of the blood, of which an excess of urates in the serum is only one of a number of phenomena, and not necessarily the sole and essential cause of the local lesions, then the question of diagnosis involves a consideration of all the correlated morbid conditions which are so frequently associated in gouty persons and gouty families as to justify the inference that they have a common origin in a perverted nutrition, the essential nature of which is imperfectly understood.

The very existence of the terms gouty rheumatism and rheumatic gout which are in common use shows that what is regarded by many excellent authorities as the confounding of distinct entities must have some foundation in clinical experience. If we consider gout, in its strictest pathological sense, acute inflammatory rheumatism, rheumatoid arthritis, or gouty rheumatism, and senile arthritis or the arthritis deformans and gonorrhoeal rheumatism as separate and distinct diseases, we shall find ourselves compelled to ignore certain common clinical facts which indicate a bond of union between them. Heredity, for example, is common to them all, and more than this, there appears to be a tendency to a differentiation of the taint in families. It is well known, for instance, that the children of gouty parents are especially liable to acute rheumatism, and acute rheumatism in youth is often followed by gout in later years. It is also a fact of common experience that while the men in gouty families are the victims of true gout, the women are apt to be the subjects of rheumatoid arthritis. The arthritis deformans which develops with the degenerations of advancing years is not infrequently associated with a family history of genuine gout. Gonorrhoeal rheumatism also, according to the experience of many trustworthy observers, often recognizes an inheritance to gouty lesions. But it is not alone in heredity and the differentiation of the type of the disease in families that the unity of these affections displays itself. The same disturbances of digestion which characterize the history of true gout are observed in those who are liable to acute rheumatism, to rheumatoid arthritis, and to arthritis deformans. It is true that excesses in food and fermented liquors do not determine, as in gout, attacks of acute rheumatism nor of the chronic forms of arthritis, for these latter diseases are commonly due to causes operating upon the nervous system, as exposure to cold and dampness or to physical or emotional shock of some kind; still, there is in the subjects of these diseases a more or less marked tendency to the same dyspeptic disorders, and especially to the diminished capacity in digesting the carbohydrates, which the subjects of true gout exhibit. In the diagnosis of gout, therefore, it would seem that the question of differentiating this disease from those which simulate it is not one in which we are called upon to distinguish one morbid entity from another, as typhus from typhoid fever or syphilis from cancer, but rather to determine, first, the presence of a recognized constitutional vice; and, secondly, to differentiate the variety of the lesions by which this vice manifests itself.

In the diagnosis of the gouty dyscrasia the first point to determine is that of heredity. This requires a careful inquiry into collateral as well as direct descent, and does not necessarily involve the discovery of arthritic diseases in the ancestors, though these are doubtless the most striking and trustworthy proofs; but the tradition in the family of persistent dyspepsia, or what is commonly called biliousness, of chronic catarrhal affections of the skin and mucous membranes, and of the chronic forms of renal disease, are significant indications of this dyscrasia. In the personal history the evidences of the lithæmic tendency, as indicated by the characteristic dyspeptic symptoms which have been described, and especially by the feeble capacity for the digestion of carbohydrates, are of great diagnostic value.

The diagnosis of gouty joint-lesions, whether acute or chronic, depends partly upon the determination of the gouty dyscrasia, and partly upon the differential distinctions which separate gouty inflammations from acute rheumatism, rheumatoid arthritis, and from the arthropathies which result from traumatism and from lesions of nerves and nerve-centres.

Gouty arthritis may be distinguished from acute rheumatism by the fact that it is more often hereditary—that it occurs in older subjects, attacking generally the smaller joints, and, as a rule, in the acute form, localizing itself in one or two joints. It is also noteworthy that the constitutional symptoms are not as severe as in rheumatism. Gout deforms the joints, while acute rheumatism leaves no traces of the inflammatory process. In addition to these distinctions there is, according to Garrod, the crucial test of an excess of urates in the blood-serum.

From rheumatoid arthritis or rheumatic gout, gout in its acute and regular form is distinguished by the more acute local and constitutional symptoms. Gout is periodical in its attacks, while rheumatoid arthritis is progressive. It attacks the smaller joints or those most exposed to strain, while rheumatoid arthritis occurs in the large as well as the small joints, and appears to be more independent of traumatism as an exciting cause. Gout is more common in men, rheumatoid arthritis in women. According to Garrod and other excellent authorities, deposits of urates are never found in the joints in rheumatoid arthritis, and there is no excess of urates in the blood. This statement is denied by Hutchinson. Ulcerations of cartilages, contractions of tendons, atrophies of muscles with subluxations of joints, are more common in rheumatoid arthritis than in gout.

While these local distinctions are undeniable, it is proper to observe that in rheumatoid arthritis the constitutional symptoms of the gouty dyscrasia, especially the dyspeptic derangements and the nervous disturbances, are often well marked; and it should also be noted that the principal distinction, the absence of urates in the blood and in the diseased joints, is one that is based on the exclusive theory that uric acid is the materies morbi of true gout. If, as is still maintained by some excellent authorities, uric acid is not essential to gout, then it must be confessed that the other distinctions are purely lesional, and that the common constitutional symptoms suggest that these diseases are divergent branches of a single trunk.